Dehydroepiandrosterone increases synaptosomal glutamate release and improves the performance in inhibitory avoidance task

被引:22
作者
Lhullier, FLR [1 ]
Nicolaidis, R [1 ]
Riera, NG [1 ]
Cipriani, F [1 ]
Junqueira, D [1 ]
Dahm, KCS [1 ]
Brusque, AM [1 ]
Souza, DO [1 ]
机构
[1] Univ Fed Rio Grande do Sul, Inst Ciencias Basicas Saude, Dept Bioquim, BR-90035 Porto Alegre, RS, Brazil
关键词
dehydroepiandrosterone; synaptosomal glutamate release; L-[H-3]glutamate uptake;
D O I
10.1016/j.pbb.2003.12.015
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Dehydroepiandrosterone (DHEA) exerts multiple effects in the rodent central nervous system (CNS), mediated through its nongenomic actions on several neurotransmitter systems, increasing neuronal excitability, modulating neuronal plasticity and presenting neuroprotective properties. It has been demonstrated that DHEA is a potent modulator of GABA(A), NMDA and Sigma receptors. In the present study, we investigated the effect of DHEA on (i) basal- and K+-stimulated L-[H-3]glutamate release from synaptosomes (both in vitro and ex vivo), (ii) synaptosomal L-[H-3]glutamate uptake (in vitro), and (iii) an inhibitory avoidance task (in vivo). The results indicated that DHEA in vitro increased glutamate release by 57%, and its intracerebroventricular infusion increased the basal[3 H]glutamate release by 15%. After 30 min of intraperitoneal administration, DHEA levels in the serum or CSF increased 33 and 21 times, respectively. Additionally, DHEA, intraperitoneally administrated 30 min before training, improved memory for inhibitory avoidance task. Concluding, DHEA could improve memory on an inhibitory avoidance task, perhaps due to its ability to physiologically strength the glutamatergic tonus by increasing glutamate release. (C) 2004 Published by Elsevier Inc.
引用
收藏
页码:601 / 606
页数:6
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